Approximately one million people per year have cardiac arrests in the United States. Less than ten percent of these people are discharged from the hospital alive without neurologic damage. This percentage of people discharged would be increased if the treatment available after the onset of cardiac arrest was improved. Five areas in which the treatment could be improved include: 1) artificial circulation during cardiopulmonary resuscitation (CPR), 2) defibrillation countershock techniques, 3) cardiac pacing, 4) cardiac monitoring, and 5) induction and maintenance of hypothermia.
The blood of a cardiac arrest patient is artificially circulated during CPR by cyclically compressing the chest. One major theory describing how artificial circulation is generated during CPR states that compression of the chest causes global increases in intrathoracic pressure. This increase in intrathoracic pressure in the thoracic compartment is evenly distributed throughout the lungs, the four chambers of the heart, as well as the great vessels in the chest. This increase in thoracic pressure becomes greater than in the compartments above and below the chest. These compartments mainly include the neck and head above the chest and the abdominal compartment below the diaphragm and chest. When thoracic pressure is increased above the pressures in these compartments, blood within the thoracic cavity moves to the head and abdomen with greater blood flow going towards the head. When the chest is released, the pressure within the thoracic cavity drops and becomes less than pressure within the head and abdomen, therefore, allowing blood to return to the thoracic cavity from the head and abdominal compartments. This theory of CPR-produced blood flow is termed the thoracic pump mechanism, whereby the entire thorax itself acts as a pump with the heart itself acting as a passive conduit for blood flow. This theory is different from the cardiac pump theory which states that compression of the chest produces blood flow by compressing the heart between the sternum and anterior structures of the vertebral column. In most patients, blood flow produced during chest compressions is likely a combination of the two theories. In each individual patient, blood flow during CPR depends on various factors such as body habitus, with thinner individuals relying more on the cardiac pump mechanism of blood flow and larger individuals with increased anterior-posterior chest dimension relying on the thoracic pump mechanism. Both mechanisms of blood flow have been shown to be present in animal and human studies. Regardless of which mechanism is invoked, currently performed standard chest compressions as recommended by the American Heart Association produces 30% or less of the normal cardiac output. This results in extremely poor regional cerebral and myocardial blood flow during CPR. This level of blood flow is usually insufficient to restart the heart and prevent neurologic damage. The purpose of CPR is to attempt to sustain the viability of the heart and brain until more definitive measures such as electrical countershock and/or pharmaco-therapy is administered to the patient.
Several techniques have been developed to take advantage of the thoracic pump mechanism of CPR-produced blood flow. One of these is the technique of simultaneous ventilation compression CPR (SVC-CPR). This technique involves inflating the lungs simultaneously during the chest compression phase of CPR. This causes larger increases in intrathoracic pressure than external chest compression alone without ventilation or ventilation alone without external chest compression. This has been shown in animal studies to result in higher cerebral blood flows than conventionally performed CPR. However, one major drawback is that coronary perfusion pressures are not uniformly increased and in some instances can be detrimentally decreased. Coronary perfusion pressure (CPP) is defined as the mean diastolic aortic pressure minus the mean diastolic right atrial pressure, and is the driving force of myocardial blood flow during CPR. When SVC-CPR was tested in a clinical trial no increase in survival was noted over standard CPR.
Another technique developed to take advantage of the thoracic pump mechanism of CPR is termed vest-CPR. This technique utilizes a bladder-containing vest analogous to a large blood pressure cuff and is driven by a pneumatic system. It is illustrated in U.S. Pat. No. 4,928,674. The vest is placed around the thorax of the patient. This pneumatic system forces compressed air into and out of the vest. When the vest is inflated, a relatively uniform decrease in the circumferential dimensions of the thorax is produced which creates an increase in intrathoracic pressure. Clinically this vest apparatus is cyclically inflated 60 times per minute with 100-250 mm of mercury pressure which is maintained for 40-50% of each cycle, with the other portion of the cycle deflating the vest to 10 mm of mercury. Positive pressure ventilation is performed independent of the apparatus after every fifth cycle. When studied clinically in humans and compared with manually performed standard external CPR, the vest apparatus produces significantly higher coronary perfusion pressure and significantly higher mean aortic, peak aortic and mean diastolic aortic pressures. However, these changes are not uniformly seen in all patients. Of note, when the vest has been studied in the laboratory and clinical settings, larger doses of epinephrine have been used to achieve these higher coronary perfusion pressures since the thoracic pump model would predict aortic, diastolic and right atrial diastolic pressures to be equivalent during the relaxation phase (when coronary perfusion occurs). No active deflation of the vest takes place, rather it is allowed to passively deflate. When this device is used, countershocks are performed by externally placed, self-adhesive defibrillator/pacer/monitor pads which are placed between the vest and skin of the patient.
Another new technique which takes some advantage of both the thoracic and cardiac pump mechanism of blood flow is called active compression-decompression CPR (ACDC-CPR). This technique utilizes a plunger-type device that is placed on the patient's sternum during cardiac arrest. The person performing chest compressions presses on this device which causes downward excursion of the anterior chest wall. What is unique is that the person then pulls up on the device. Since the device is attached to the sternum by suction, this causes the anterior chest to be actively recoiled instead of undergoing the usual passive recoil of standard external CPR. This active recoil is capable in many individuals of causing a decrease in intrathoracic pressure which is transmitted to the right atrium, thus lowering right atrial pressure during artificial diastole and in turn increasing coronary perfusion pressure. This negative pressure also has the effect of increasing venous return to the thoracic cavity which may enhance cardiac output. This negative pressure also may cause movement of air into the lung which may create some artificial ventilation. Factors such as body habitus and chest compliance which impact on the efficacy of ACDC-CPR have not been studied but are likely to have an effect. Persons with larger body habitus would receive less benefit from the technique.
In addition to artificial circulation, many patients also require a defibrillation countershock during CPR in order to re-start their heart. Defibrillation countershock therapy involves placing two electrodes near the heart and inducing a flow of electrical current through the chest and heart, and preferably through the left ventricle of the heart, which is the largest portion of the heart muscle that is fibrillating. The electrodes used have conventionally been hand-held paddles or adhesive pads, either of which are placed at different positions on the external surface of the patient's chest, sides and/or back. A defibrillation countershock with this electrode placement methodology is commonly called an external defibrillation countershock.
A sufficient electrical current density must be induced in the myocardium in order to defibrillate a fibrillating heart. Current density is defined as the amount of current per cross-sectional area of tissue. In addition, this required minimum current density must depolarize a certain minimum critical mass of the left ventricle of the heart in order to achieve defibrillation. For any given total current induced in the chest during a defibrillation countershock, the current density in the myocardium is generally inversely proportional to the distance between the countershock electrodes. This distance will vary depending on the location of the electrodes and the size of the patient's chest. If the electrodes are widely separated, more of the total current will pass through non-myocardial tissue. It is, therefore, advantageous to position the electrodes as close to the heart as possible in order to achieve defibrillation.
The machine used to deliver a defibrillation countershock as well as monitor and, when necessary, pace a patient's heart, is commonly called a defibrillator/pacer/monitor. All defibrillators today are clinically described as energy defibrillators in that the person administering countershock therapy presets the amount of electrical energy to be delivered to the patient during the countershock. For any preset energy level and electrode distance, the total current and current density induced in the myocardium is generally inversely proportional to the electrical impedance of the tissue lying between the electrodes. Although the myocardium has a relatively low impedance to electrical flow, tissue such as bone has a high impedance. For instance, structures such as the sternum, ribs and vertebral column have relatively high impedances to current flow. Some or all of these tissues, including skin, fat and cartilage, interpose the electrodes during the external countershock. It is, therefore, advantageous to position the electrodes so that there is the least possible amount of non-myocardial high impedance tissue between them.
It is further advantageous to use the smallest amount of current necessary to defibrillate the heart of the patient in cardiac arrest. Excessive current may cause irreversible structural damage to the myocardial tissue.
Conventional, internal countershock therapy utilizes the most ideal electrode placement and offers the highest probability of achieving defibrillation. In this method, the pair of electrodes is placed on opposite sides of and touching the left ventricle of the exposed heart, and the current is induced between the two electrodes. Under this circumstance, the distance between the electrodes is minimized and virtually no other tissues other than the myocardium interpose the electrodes. Virtually all the current flows through the left ventricle of the heart. This electrode placement requires the chest be open in order to expose the heart. Therefore, it is typically only performed under sterile conditions in an operating room. The procedures are impractical in an emergency setting outside the operating room.
There are several newly proposed methods of electrode placement meant to reduce the amount of high impedance tissue between the electrodes as well as reduce the distance between the electrodes. These involve placing one or more electrodes in the esophagus, stomach, esophagus and external chest, esophagus and stomach (patent pending) and esophagus, stomach, and external chest (patent pending). Examples of some of these are shown in U.S. Pat. Nos. 4,198,963 and 5,197,491 and PCT Application WO 92/06681. None of these proposed electrode orientations are directly in contact with the visceral or parietal surfaces of the thoracic cavity, lung or heart.
Patients suffer respiratory failure for numerous reasons. Normal respiration controlled by the brain is achieved by contraction and relaxation of respiratory muscles such as the diaphragm and intercostal muscles. The contraction of these muscles helps to produce negative intrathoracic pressures which draws air into the lungs. Relaxation of these muscles produces passive recoil of the chest and exhalation. During cardiac arrest when brain blood flow is insufficient, neural control of the respiratory muscles is lost. In states of trauma and other diseases, chest and lung compliance decreases which can cause fatigue of the respiratory muscles. When respiratory failure occurs, artificial ventilation is usually required by the technique of positive pressure ventilation. This usually requires endotracheal intubation. Positive pressure ventilation does not use negative pressure. Artificial means of ventilation by altering intrathoracic pressures by producing negative intrathoracic pressures might be advantageous and may reduce the need for endotracheal intubation. During standard external CPR and ACDC-CPR, it has been shown that if chest excursion is large enough, positive pressure ventilation may not be required for some time period.
One of the few resuscitative interventions found to improve neurologic outcome from cardiac arrest is induction and maintenance of cerebral hypothermia in the post resuscitation period. Although shown to be very effective, it is extremely difficult to rapidly produce a state of resuscitative hypothermia within a time frame immediately after restoration of spontaneous circulation following cardiac arrest. Although a decrease in cerebral temperature from 37.degree. to 34.degree. C. has proven to be neuro-protective, even this small drop of 3 degrees is difficult to produce rapidly. In order to be effective this mild degree of hypothermia must be produced within minutes of the resuscitation. Methods such as isolated head cooling by placement of the head in an ice bath or by nasopharyngeal cooling, injection of the carotid circulation with cooled solution, thoracic and peritoneal lavage, placement of the head and thorax in a cooling helmet and jacket, are all problematic in that hypothermia is not attained rapidly enough, or if attained cannot be maintained for a sufficient duration of time to be neuro-protective. Although cardiopulmonary bypass can produce a state of therapeutic hypothermia very rapidly, its institution either with traditional placement through a median sternotomy or through peripheral placement percutaneously via the femoral artery and femoral vein, is too time-consuming for it to be of practical use in the emergency setting. Thoracic and peritoneal lavage, although effective, are also somewhat time-consuming and cumbersome in the emergency setting especially when ongoing resuscitative efforts are required. Carotid flush is effective but would involve needle or catheter placement in the internal carotid artery which may be impractical, difficult to achieve, or unsafe. Although almost immediate brain cooling can be achieved with carotid flushing, once restoration of spontaneous circulation is achieved, continuous infusion would be required to maintain cerebral hypothermia. Cooling jackets and cooling helmets along with placement of the head in an ice bath require too long of a time period to be effective in rapidly reducing the cerebral temperature. The main problem with these techniques is that if cooling is not simultaneously accompanied by sufficient cerebral blood flow, rapid temperature drops are unlikely to occur. This is especially true of external cooling because the amount of blood flow and temperature gradient that would be required to cause rapid drops in core temperature is quite large. The same problems exist when attempting to rapidly induce hypothermia in victims of head trauma.
Therapeutic measures which have been shown to aid victims of head trauma include induction of therapeutic hypothermia and reductions in intracranial pressure. Hypothermia has been shown to improve the survival and reduce the amount of injured neurologic tissue. Several proposed mechanisms by which this happens are decreases in the metabolic requirements of the injured tissue, as well as decreases in the secretion of damaging neurotransmitters by the injured tissue. Currently the main mechanisms for reducing intracranial pressure involve the administration of diuretics such as furosemide and mannitol, administration of steroids which reduce swelling, removal of cerebral spinal fluid, elevation of the head which promotes venous drainage, administration of barbiturates which reduce the metabolic demand of brain tissue, hyperventilation producing hypocapnia and reduced cerebral blood flow which decrease intracranial pressure, and as a last resort, removal of less necessary parts of the brain itself. Production of hypothermia in head-injured patients has been limited to cooling blankets which produce whole body cooling. Although sometimes effective, whole body cooling is difficult to initiate early.
Prolonged exposure to cold or hot environments under certain conditions can result in life-threatening states of hypo- or hyperthermia, respectively. Patients may present in various forms of shock and/or various forms of altered mental status. In cases of hypothermia, an attempt is made to normalize the core body temperature as rapidly as possible. Methods have included passive rewarming with blankets and heating lamps, cardiopulmonary bypass, infusion of warmed intravenous fluids, peritoneal, bladder, gastric, thoracic, and mediastinal lavage, and breathing of warmed humidified air. Many of these methods are ineffective and are capable of only raising core temperature at a rate of 1.degree. C. an hour. Some will be rendered totally ineffective based on the victim's circulatory status. Others such as peritoneal and thoracic lavage with warmed fluids are effective but time-consuming and difficult to control. In addition, they cannot help support the circulation during shock. Cardiopulmonary bypass is effective but is time-consuming and requires an extensive level of expertise.
Treatment of hyperthermic emergencies requires the ability to rapidly lower the body's core temperature to normal to avoid shock, cardiac arrest, and various forms of neurologic damage. Methods currently used are moderately effective and include ice packing, lavage of various body cavities with cooled fluids, and convection with water spray and fanning. Some of the methods will be totally ineffective based on the status of the patient's circulation. In addition, if countershock or pacing is required, safety hazards are present if the surface of the body is wet from the cooling technique used. In addition, none of the above methods will be capable of simultaneously supporting the circulation.